Our over-all objective is to test a theoretical model developed to account for the phenomenon of increased longevity in irradiated insects. The model's major tenet is that radiation damage to DNA induces higher levels of DNA-repair enzymes which would otherwise decline in differentiated postmitotic tissues. Enzymes which repair radiation-damaged DNA also participate in repair of DNA damaged by chemicals, including, presumably, some metabolic products. Thus, the model predicts: DNA-damaging chemicals should increase longevity in insects (and other predominantly postmitotic organisms); nonrepairable damage, such as that from high LET radiations, should be effective, in the manner of gratuitous inducers; there should be age-related declines in resistance to two types of deleterious agents: those which damage DNA in differentiated tissues and those whose effects must be overcome by transcribing genetic information encoded in such tissues. Experimental approaches include testing for effects of DNA-damaging chemicals, psoralen plus near UV, and high-LET radiations on insect longevity, and examining influence of age and of prior irradiation on thermal tolerance, temperature acclimation, and resistance to oxygen poisoning and to chronic physical stress.